| Systematic (IUPAC) name | |
|---|---|
| N2-acetyl-N-benzyl-D-homoserinamide | |
| Clinical data | |
| Trade names | Vimpat |
| AHFS/Drugs.com | monograph |
| MedlinePlus | a609028 |
| Pregnancy cat. | ? |
| Legal status | Schedule V (U.S.) |
| Routes | Oral, intravenous |
| Pharmacokinetic data | |
| Bioavailability | High |
| Half-life | 13 hours |
| Identifiers | |
| CAS number | 175481-36-4 |
| ATC code | N03AX18 |
| PubChem | CID 219078 |
| ChemSpider | 189902 |
| UNII | 563KS2PQY5 |
| KEGG | D07299 |
| ChEMBL | CHEMBL58323 |
| Synonyms | (2R)-2-(acetylamino)-N-benzyl-3-methoxypropanamide |
| Chemical data | |
| Formula | C13H18N2O3 |
| Mol. mass | 250.294 g/mol |
| SMILES | eMolecules & PubChem |
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Lacosamide (INN, formerly known as erlosamide) is a medication developed by UCB for the adjunctive treatment of partial-onset seizures and diabetic neuropathic pain marketed under the trade name Vimpat.
The U.S. Food and Drug Administration accepted UCB's New Drug Application for lacosamide as of November 29, 2007, beginning the approval process for the drug.[1][2] UCB also filed for marketing approval in the European Union; the European Medicines Agency accepted the marketing application for review in May 2007.[1][3]
The drug was approved in the EU on September 3, 2008.[4] It was approved in the US on October 29, 2008.[5] Lacosamide release was delayed owing to an objection about its placement into schedule V of the Controlled Substances Act. The FDA issued their final rule of placement into Schedule V on June 22, 2009[6].
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Lacosamide is a functionalized amino acid that has activity in the maximal electroshock seizure test, like antiepileptic drugs that are believed to act through voltage-gated sodium channels[7]. However, lacosamide does not act in a conventional way to stabilize fast sodium channel inactivation. Rather, recent studies indicate that it enhances slow inactivation[8] . During an action potential voltage gated sodium channels undergo fast inactivation. This inactivation prevents the channel from opening, and helps end the action potential. Many antiepileptic drugs, like carbamazepine or lamotrigine, slow the recovery from inactivation and hence reduce the ability of neurons to fire action potentials. Inactivation only occurs in neurons firing action potentials, this means that drugs that modulate fast inactivation selectively reduce the firing in active cells. Slow inactivation is similar but does not produce complete blockade of voltage gated sodium channels, with both activation and inactivation occurring over hundreds of milliseconds or more. Lacosamide makes this inactivation happen at less depolarized membrane potentials. This means that lacosamide only effects neurons which are depolarized or active for long periods of time, typical of neurons at the focus of an epileptic focus.[8]
Lacosamide does not affect AMPA, kainate, NMDA, GABAA, GABAB or a variety of dopaminergic, serotonergic, adrenergic, muscarinic or cannabinoid receptors and does not block potassium or calcium currents [9]
In a large double-blind, randomized clinical trial of people with poorly controlled partial-onset seizures, lacosamide was found to significantly reduce seizure frequency when given in addition to other antiepileptics, at doses of 400 and 600 milligrams a day.[10] In a smaller trial of people with diabetic neuropathy, lacosamide also provided significantly better pain relief when compared to placebo.[11]
Lacosamide was generally well tolerated in adult patients with partial-onset seizures. Dizziness was the most common treatment-related adverse event.[12]
J.A. McIntyre, J. Castaner, Drugs Future 29, 992 (2004).
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